Transient forebrain ischemia depletes glucose and oxygen levels in the brain. In this pathological condition, lactate serves an important role in cellular metabolism as the end product of glycolysis. The present study investigated the expression of monocarboxylate transporter 4 (MCT4) in lactate metabolism in the hippocampal CA1 region following induction of transient forebrain ischemia. MCT4 immunoreactivity was detected in CA1 pyramidal cells of the sham-operated group. Animals from the ischemic group exhibited a transient decrease in MCT4 immunoreactivity in the CA1 region between 30 min and 3 h following ischemia compared with the sham‑operated group. The initial decrease in immunoreactivity observed between 30 min and 3 h following ischemia was followed by an increase at 2 days after the treatment. A significant increase in MCT4 immunoreactivity levels was observed 2 days after ischemia compared with the sham‑operated group. Limited MCT4 immunoreactivity was observed in the pyramidal neurons 3 days after ischemia. At 4‑10 days after ischemia, MCT4 immunoreactivity was detected in the strata radiatum, oriens and pyramidale. Furthermore, MCT4 immunoreactivity levels in the CA1 region exhibited a time‑dependent increase following ischemia. The results indicated that there were transient alterations observed in the localization of MCT4 following the induction of ischemia, and further studies are required to investigate the association between MCT4 expression and lactate metabolism in providing energy to the post‑ischemic brain.
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